PUBLICATION
Neuroepithelial oxygen chemoreceptors of the zebrafish gill
- Authors
- Jonz, M.G., Fearon, I.M., and Nurse, C.A.
- ID
- ZDB-PUB-040908-3
- Date
- 2004
- Source
- The Journal of physiology 560(Pt 3): 737-52 (Journal)
- Registered Authors
- Jonz, Michael G.
- Keywords
- chemoreceptor, hypoxia, patch-clamp
- MeSH Terms
-
- Animals
- Chemoreceptor Cells/physiology*
- Gills/drug effects
- Gills/pathology
- Gills/physiology*
- Hypoxia, Brain/physiopathology
- In Vitro Techniques
- Membrane Potentials/drug effects
- Membrane Potentials/physiology
- Neuroepithelial Cells/drug effects
- Neuroepithelial Cells/pathology
- Neuroepithelial Cells/physiology*
- Oxygen/physiology*
- Quinidine/pharmacology
- Zebrafish/physiology*
- PubMed
- 15331683 Full text @ J. Physiol.
Citation
Jonz, M.G., Fearon, I.M., and Nurse, C.A. (2004) Neuroepithelial oxygen chemoreceptors of the zebrafish gill. The Journal of physiology. 560(Pt 3):737-52.
Abstract
In aquatic vertebrates, hypoxia induces physiological changes that arise principally from O2 chemoreceptors of the gill. Neuroepithelial cells (NECs) of the zebrafish gill are morphologically similar to mammalian O2 chemoreceptors (e.g. carotid body), suggesting that they may play a role in initiating the hypoxia response in fish. We describe morphological changes of zebrafish gill NECs following in vivo exposure to chronic hypoxia, and characterize the cellular mechanisms of O2 sensing in isolated NECs using patch-clamp electrophysiology. Confocal immunofluorescence studies indicated that chronic hypoxia (PO2 = 35 mmHg, 60 days) induced hypertrophy, proliferation and process extension in NECs immunoreactive for serotonin or synaptic vesicle protein (SV2). Under voltage clamp, NECs responded to hypoxia (PO2 = 25-140 mmHg) with a dose-dependent decrease in K(+) current. The current-voltage relationship of the O2-sensitive current (IKO2) reversed near EK and displayed open rectification. Pharmacological characterization indicated that IKO2 was resistant to 20 mM TEA and 5 mM 4-AP, but was sensitive to 1 mM quinidine. In current-clamp recordings, hypoxia produced membrane depolarization associated with a conductance decrease; this depolarization was blocked by quinidine, but was insensitive to TEA and 4-AP. These biophysical and pharmacological characteristics suggest that hypoxia sensing in zebrafish gill NECs is mediated by inhibition of a background K(+) conductance, which generates a receptor potential necessary for neurosecretion and activation of sensory pathways in the gill. This appears to be a fundamental mechanism of O2 sensing that arose early in vertebrate evolution, and was adopted later in mammalian O2 chemoreceptors.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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